Gene interactions and pathways from curated databases and text-mining

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SMAD1 — SMAD5

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Harada et al., J Biol Chem 2003 : HIPK2 efficiently inhibited Smad1/4 induced transcription from the Smad site containing promoter
Fuller et al., Ann Neurol 2007 (Demyelinating Diseases...) : Cultured mature astrocytes respond directly to BMPs with Smad1 translocation to the nucleus, increased phosphorylated Smad1/5/8 , and increases in glial fibrillary acidic protein and CSPG expression
Matsubara et al., J Biol Chem 2008 : Furthermore, overexpression of Smad1 and Smad4 up-regulated Osterix expression, and an inhibitory Smad , Smad6, markedly suppressed BMP2 induced Osterix expression in the Runx2-deficient cells
Wang et al., J Biol Chem 2011 : Thus, we conclude that CHIP inhibits the signaling activities of Smad1/5 by recruiting Smad1/5 from the functional R-/Co-Smad complex and further promoting the ubiquitination/degradation of Smad1/5 in a chaperone independent manner
Lv et al., Nan Fang Yi Ke Da Xue Xue Bao 2013 : Transfection of the BMSCs with Smad1 siRNA decreased the basal level of Smad1/5/8 protein expression, and also inhibited Sr-induced up-regulation of p-Smad1/5/8 and Runx2 expressions as well as Sr-induced enhancement of ALP activity and formation of mineralized nodules
Ellman et al., Gene 2013 : The synergism results from LfcinB mediated activation of Sp1 and SMAD signaling pathways by ( i ) phosphorylation of SMAD 1/5/8 ; ( ii ) downregulation of SMAD inhibitory factors [ i.e., noggin and SMAD6 ( inhibitory SMAD ) ] ; and ( iii ) upregulation of SMAD4 ( universal co-SMAD ) ... The synergism results from LfcinB mediated activation of Sp1 and SMAD signaling pathways by ( i ) phosphorylation of SMAD 1/5/8 ; ( ii ) downregulation of SMAD inhibitory factors [ i.e., noggin and SMAD6 ( inhibitory SMAD ) ] ; and ( iii ) upregulation of SMAD4 ( universal co-SMAD )